试从痰瘀论炎症

试从痰瘀论炎症天津中医学院第一附属医院（３００１９３）唐丽，曹克先主题词炎症／中医病机，炎症／中医药疗法，痰（中医）／致病力１对炎症的认识祖国医学无炎症之称，只有火性上炎之说。现代医学认为炎症是机体组织对于各种损伤性刺激发生的全身性防御反应在局部的表...

炎症与中医寒热证关系初探

炎症与中医寒热证关系初探深圳市红十字会医院（５１８０２９）李一明主题词炎症／中医病机，寒热辨证，咳嗽／分类，咳嗽／中医药疗法现代医学的炎症不少临床医师首先考虑到的是热证。属于热证的炎症固然多见，但不少炎症性疾病经中医辨证属于寒证或寒热错杂证，易被临床...

炎症浅识

炎症浅识湖南省衡东县新塘医院（４２１４１１）刘爱云，彭光辉主题词炎症／中医病机，炎症／中医药疗法１炎症的概念现代医学认为，具有血管系统的活体组织对局部损伤的反应（以损伤起始、治愈告终的复杂过程）为炎症。并指出：体表的急性炎症临床上都可见到红、肿、热、...

Etiopathogenesis of inflammatory bowel diseases

Theories explaining the etiopathogenesis of inflammatory bowel disease （IBD） have been proposed ever since Crohn＇s disease （CD） and ulcerative colitis （UC） were recognized as the two major forms of the disease. Although the exact cause（s） and mechanisms of tissue damage in CD and UC have yet to be completely understood, enough progress has occurred to accept the following hypothesis as valid： IBD is an inappropriate immune response that occurs in genetically susceptible individuals as the result of a complex interaction among environmental factors, microbial factors, and the intestinal immune system. Among an almost endless list of environmental factors, smoking has been identified as a risk factor for CD and a protective factor for UC. Among microbial factors, no convincing evidence indicates that classical infectious agents cause IBD, while mounting evidence points to an abnormal immune response against the normal enteric flora as being of central importance. Gut inflammation is mediated by cells of the innate as well as adaptive immune systems, with the additional contribution of non-immune cells, such as epithelial, mesenchymal and endothelial cells, and platelets.

Current view of the immunopathogenesis in inflammatory bowel disease and its implications for therapy

Although the aetiology of inflammatory bowel disease (IBD) remains unknown, the pathogenesis is gradually being unravelled, seeming to be the result of a combination of environmental, genetic, and immunological factors in which an uncontrolled immune response within the intestinal lumen leads to inflammation in genetically predisposed individuals. Multifactorial evidence suggests that a defect of innate immune response to microbial agents is involved in IBD. This editorial outlines the immunopathogenesis of IBD and their current and future therapy. We present IBD as a result of dysregulated mucosal response in the intestinal wall facilitated by defects in epithelial barrier function and the mucosal immune system with excessive production of cytokines growth factors, adhesion molecules, and reactive oxygen metabolites, resulting in tissue injury. Established and evolving therapies are discussed in the second part of this editorial and at the end of this section we review new therapies to modulate the immune system in patients with IBD.

Evaluation of esophageal function in patients with esophageal motor abnormalities using multichannel intraluminal impedance esophageal manometry

AIM: To evaluate the functional aspect of esophageal motility in healthy subjects and in patients who were referred for esophageal function testing using multichannel intraluminal impedance-esophageal manometry (MII-EM), and to assess the clinical utility of MII-EM. METHODS: From September 2003 to January 2004, we performed the MII-EM on healthy volunteers and all the patients who were referred for esophageal function testing. Each patient received 10 liquid and 10 viscous swallows. We analyzed the results, the impedance and the manometric findings. Some of the subjects had additional ambulatory 24-h pH study performed to diagnose gastroesophageal reflux disease (GERD). RESULTS: Among 89 studied subjects, the MII-EM findings showed normal esophageal motility in 50 (56.17%), ineffective esophageal motility (IEM) in 17 (19.10%), nutcracker esophagus in 7 (7.86%), achalasia in 4 (4.49%), and scleroderma esophagus in 11 (12.35%) cases. The completeness and the speed of bolus transit were in the order of nutcracker esophagus, normal manometry and IEM. Some of the swallows showing normal manometry and IEM had incomplete transit. In the achalasia and scleroderma esophagus, almost all the swallows had incomplete transit. The body amplitudes were higher for the swallows with complete transit than for the swallows with incomplete transit. There was not a significant difference in the manometric and impedance findings between the subjects with and without GERD. CONCLUSION: MII-EM is a useful tool in assessing theesophageal function in the patients having esophageal motility abnormality. The primary factors influencing the bolus transit are the amplitude of the esophageal body and normal peristalsis.

Crohn's disease in Stockholm County during 1990-2001:An epidemiological update

AIM： To further assess of the incidence and localization of Crohn＇s disease （CD） in a well-defined population during the 1990s and to evaluate the prevalence of CD on the 1^st of January 2002. METHODS： In a retrospective population based study, all 16-90 years old citizens of Stockholm County diagnosed as having CD according to Lennard Jones＇ criteria between 1990 and 2001 were included. Case identification was made by using computerized inpatient and outpatient registers. Moreover private gastroenterologists were asked for possible cases. The extent of the disease and the frequency of anorectal fistulae were determined as were the ages at diagnosis. Further, the prevalence of CD on the 1^st of January 2002 was assessed. RESULTS： All the 1 389 patients, 689 men and 700 women, fulfilled the criteria for CD. The mean incidence rate for the whole period was 8.3 per 10s （95%CI 7.9 -8.8）. There was no difference between the genders. The mean annual incidence of the whole study period for colorectal disease and ileocecal disease, was 4.4 （95%CI 4.0-4.7） and 2.4 （95%CI 2.1-2.6） per 10s, respectively. Perianal disease occurred in 13.7% （95%CI 11.9-15.7 %） of the patients. The prevalence of CD was 213 per 100 000 inhabitants. CONCLUSION： The incidence of CD has markedly increased during the last decade in Stockholm County and 0.2% of the population suffers from CD. The increase is attributed to a further increase of colorectal disease, while the incidence of ileocecal disease has remained stable.

Helicobacter pylori infection and respiratory diseases:a review

In the past few years,a variety of extradigestive disorders, including cardiovascular,skin,rheumatic and liver diseases, have been associated with Helicobacter pylori(H.pylori) infection.The activation of inflammatory mediators by H.pylori seems to be the pathogenetic mechanism underlying the observed associations.The present review summarizes the current literature,including our own studies,concerning the association between H.pyloriinfection and respiratory diseases. A small number of epidemiological and serologic,case- control studies suggest that H.pylori infection may be associated with the development of chronic bronchitis.A frequent coexistence of pulmonary tuberculosis and H.pylori infection has also been found.Moreover,recent studies have shown an increased H.pyloriseroprevalence in patients with bronchiectasis and in those with lung cancer.On the other hand,bronchial asthma seems not to be related with H.pylori infection. All associations between H.pylori infection and respiratory diseases are primarily based on case-control studies, concerning relatively small numbers of patients.Moreover, there is a lack of studies focused on the pathogenetic link between respiratory diseases and H.pylori infection. Therefore,we believe that larger studies should be undertaken to confirm the observed results and to clarify the underlying pathogenetic mechanisms.

Role of LPS/CD14/TLR4-mediated inflammation in necrotizing enterocolitis:Pathogenesis and therapeutic implications

AIM:To establish the roles of lipopolysaccharide (LPS)/CD14/toll-like receptor 4 (TLR4)-mediated inflammation in a rat model of human necrotizing enterocolitis (NEC).METHODS: Six pairs of intestinal samples from human NEC were collected before and after recovery for histological and molecular analysis of inflammatory cytokines and signaling components. In the rat NEC model, we isolated 10-cm jejunum segments and divided them into six groups (n=6) for sham operation, treatment with LPS, bowel distension, combined bowel distension and LPS stimulation, and two therapeutic groups. The potential eff icacy of a recombinant CD18 peptide and a monoclonal CD14 antibody was evaluated in the latter two groups. The serum and tissue levels of several inflammatory mediators were quantified by real-time polymerase chain reaction, ELISA and immunoblotting.RESULTS: Human acute phase NEC tissues displayed significant increases (P<0.05) in levels of TLR4, CD14, myeloid differentiation protein (MD)-2, tumor necrosis factor (TNF)-α and nuclear factor-κB when compared to those after recovery. The histological and inflammatory picture of human NEC was reproduced in rats that were treated with combined bowel distension and LPS, but not in the sham-operated and other control rats. Serum levels of interleukin-6 and TNF-α were also elevated. The NEC pathology was attenuated by treating the NEC rats with a monoclonal CD14 antibody or an LPS-neutralizing peptide.CONCLUSION:LPS and distension are required to produce the histological and inflammatory features of NEC. A potential treatment option is blocking LPS activation and leukocyte infi ltration.

Induction of apoptosis by artemisinin relieving the severity of inflammation in caerulein-induced acute pancreatitis

AIM： To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis （AP）, and the influences of artemisinin on them.METHODS： AP was induced by 4 intraperitoneal iojections of caerulein at 1 h intervals. To induce apoptosis, solution of artemisinin （50 mg/kg） was given intraperitoneally 1, 12, 24 and 36 h after the last caerulein injection. Histological examination of impairment of pancreatic tissue and detection of serum amylase were performed to evaluate the severity of acute pancreatitis. Apoptosis and oncosis were detected with acridine orange （AO） and ethylene dibromide （EB） staining. Caspase-3 and myeloperoxidase （MPO） activity were measured by colorimetric assay. Nuclear factor-kappa B （NF-KB） activation was detected by flow cytometry. Macrophage inflammatory protein-lα（MIP-1α） protein was measured by Western blot. Interleukin- 1β（IL-1β） mRNA was detected by RT-PCR.RESULTS： Addition of artemisinin increased the number of apoptotic cells （11.7%±1.4% vs 6.3%± 0.7%, P 〈 0.05）, while reduced the number of oncotic cells （13.0% ±2.4% vs 17.5%±2.2%, P 〈 0.05）. The activity of caspase-3 speeded up （1.52±0.21 vs 1.03±0.08, P 〈 0.05）, the pancreas pathological impairment was relieved （3.0±0.5 vs 4.0± 0.5, P 〈 0.05） and the level of serum amylase decreased （5642±721 U/dL vs 7821±653 U/dL, P 〈 0.05）. The activation of NF-1α （29%±4.1% vs 42%±5.8%）, MIP-1α protein （3.7±0.5 vs 5.8±0.7）,MPO （0.52±0.06 U/g vs 0.68±0.09 U/g）, IL-1β mRNA （1.7 ±0.3 vs 2.4 ±0.4） in the apoptosis inducing group was obviously decreased （P 〈 0.05）.CONCLUSION： Inducing apoptosis can relieve pathological impairment and inflammatory reaction in AP rats.

Gastric sarcoidosis mimicking irritable bowel syndrome-Cause not association?

Sarcoidosis is a systemic disease of unknown aetiology that may affect any organ in the body. The gastrointestinal tract however is only rarely affected outside the liver. Symptoms may be non-specific. Irritable bowel syndrome （IBS） is a common diagnosis. The recognition of IBS is aided by the use of the Rome Ⅱ criteria-in the absence of organic disease. We describe the first case of a patient with gastric sarcoidosis who presented with IBS symptoms but subsequently responded to immunosuppressive therapy.

Current concept on the pathogenesis of inflammatory bowel disease-crosstalk between genetic and microbial factors:Pathogenic bacteria and altered bacterial sensing or changes in mucosal integrity take"toll"?

The pathogenesis of inflammatory bowel disease （IBD） is only partially understood. Various environmental and host （e.g. genetic-, epithelial-, immune and nonimmune） factors are involved. It is a multifactorial polygenic disease with probable genetic heterogeneity. Some genes are associated with IBD itself, while others increase the risk of ulcerative colitis （UC） or Crohn＇ s disease （CD） or are associated with disease location and/or behaviour. This review addresses recent advances in the genetics of IBD. The article discusses the current information on the crosstalk between microbial and genetic factors （e.g. NOD2/CARD15, SLC22A46A5 and DLG5）. The genetic data acquired in recent years help in understanding the pathogenesis of IBD and can identify a number of potential targets for therapeutic intervention. In the future, genetics may help more accurately diagnose and predict disease course in IBD.

Effect of admission hypertriglyceridemia on the episodes of severe acute pancreatitis

AIM： To investigate the effect of admission hypertriglyceridemia （HTG） on the episodes of severe acute pancreatitis （SAP）. METHODS： One hundred and seventy-six patients with SAP were divided into HTG group （n = 45） and control group （n = 131） according to admission triglyceride （TG） ≥ 5.65 mmol/L and 〈 5.65 retool/L, respectively. Demographics, etiology, underlying diseases, biochemical parameters, Ranson＇ s score, acute physiology and chronic heath evaluation Ⅱ （APACHE Ⅱ） score, Balthazar＇s computed tomography （CT） score, complications and mortality were compared. Correlation between admission TG and 24-h APACHE Ⅱ score was analyzed. RESULTS： SAP patients with HTG were younger （40.8 ± 9.3 years vs 52.6 ± 13.4 years, P 〈 0.05） with higher etiology rate of overeating, high-fat diet （40.0% vs 14.5%, P 〈 0.05） and alcohol abuse （46.7% vs 23.7%, P 〈 0.01）, incidence rate of hypocalcemia （86.7% vs 63.4%, P 〈 0.01） and hypoalbuminemia （84.4% vs 60.3%, P 〈 0.01）, 24-h APACHE Ⅱ score （13.6 ± 5.7 vs 10.7 ± 4.6, P 〈 0.01） and admission serum glucose （17.7 ± 7.7 vs 13.4 ± 6.1, P 〈 0.01）, complication rate of renal failure （51.1% vs 16.8%, P 〈 0.01）, shock （37.9% vs 14.5%, P 〈 0.01） and infection （37.4% vs 18.3%, P 〈 0.01） and mortality （13.1% vs 9.1%, P 〈 0.01）. Logistic regression analysis showed a positive correlation between admission TG and 24-h APACHE Ⅱ score （r = 0.509, P = 0.004）.CONCLUSION： The clinical features of SAP patients with HTG are largely consistent with previous studies, HTG aggravates the episodes of SAP.

Cerebral sinus thrombosis in patients with inflammatory bowel disease: A case report

Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease of the gastrointestinal tract. The pathophysiology of IBD is probably the result of the complex interaction of genetic susceptibility and environmental influences. There is a well-known risk of thrombosis in patients with IBD. We present the case of a 53-year-old man with ulcerative colitis, who spontaneously developed intracranial sinus thrombosis that was treated with low molecular weight heparin. Literature was searched to assess the frequency and characteristics of cerebral sinus thrombosis in IBD and the role of certain etiopathological factors in such thrombotic patients.

Diverticular disease of the colon:New perspectives in symptom development and treatment

Diverticular disease of the colon is a common disease worldwide.Although the disease is asymptomatic in about 70-80 % of patients,it represents,at least in Western countries,one of the most important gastrointestinal diseases in terms of direct and indirect health costs.Pathogenesis of the disease is still unknown.However,it is the result of complex interactions between colonic structure,intestinal motility,diet and genetic factors.Whilst efficacious preventive strategies remain to be identified,fibre supplementation in the diet is recommended.Why symptoms develop is still unclear.Results of recent experimental studies on irritable bowel syndrome speculated that low grade inflammation of colonic mucosa,induced by changes in bacterial microflora, could affect the enteric nervous system,which is crucial for normal gut function,thus favouring symptom development. This hypothesis could be extrapolated also for diverticular disease,since bacterial overgrowth is present,at least in a subgroup of patients.These perspectives on symptom development are reviewed and new therapeutic approaches are hypothesized.

Indications for 5-aminosalicylate in inflammatory bowel disease:Is the body of evidence complete?

Mesalazine is a safe drug, although adverse events may be seen in a minority of patients. This applies also to pregnant women and children. The role of mesalazine in combination therapy to improve efficacy and con- comitant drug pharmacokinetics, or in chemoprevention against inflammatory bowel disease (IBD)-related co- lonic carcinoma has not yet been completely elucidated. Therapeutic success of mesalazine may be optimized by a combination of high dose and low frequency of dos- age to improve compliance. Therefore, due to its supe- rior safety profile and pharmacokinetic characteristics, mesalazine is preferable to sulphasalazine. This paper reviews the literature concerning mechanisms of action, indications and off-label use, pharmacokinetic properties and formulations, therapeutic efficacy, compliance, pae- diatric indications, chemoprevention, and safety issues and adverse event profile of mesalazine treatment versus sulphasalazine. It also highlights these controversies in order to clarify the potential benefits of mesalazines in IBD therapy and evidence for its use.

Difficulty with diagnosis of malignant pancreatic neoplasms coexisting with chronic pancreatitis

Chronic pancreatitis is a relatively common disease. We encountered two different cases of belatedly demonstrated pancreatic carcinoma featuring underlying chronic pancreatitis. The first case was one that was highly suspected as that of a malignancy based upon imaging study, but unfortunately, it could not be confirmed by intra-operative cytology at that time. Following this, the surgeon elected to perform only conservative bypass surgery for obstructive biliary complication. Peritoneal carcinomatosis was later noted and the patient finally died. The second case, a malignant mucinous neoplasm,was falsely diagnosed as a pseudocyst, based upon the lesion's sonographic appearance and associated elevated serum amylase levels. After suffering repeated hemoptysis,the patient was found to exhibit lung metastasis and peritoneal seeding. We reviewed some of the literature,including those studies discussing chronic pancreatitis predisposing to a malignant change. These two case analyses illustrate clearly that the diagnosis for such conditions, which is simply based upon imagery or pathological considerations may end up being one of a mistaken malignancy. Some of our suggestions for the treatment of such malignancies as revealed herein include,total pancreatomy for univocal mass lesion, and needle aspiration of lesion-contained tissue for amylase, CA199and CEA levels for a suspicious cystic pancreatic mass.

Clinical characteristics of fulminant hepatitis in pregnancy

AIM： To investigate the clinical characteristics of fulminant hepatitis in pregnancy. METHODS： We compared and analyzed the etiology, clinical characteristics, and laboratory examinations of 25 cases of fulminant hepatitis in pregnancy and 30 cases of fulminant hepatitis not in pregnancy. RESULTS： HBV infection and chronic fulminant hepatitis were most common both in the pregnant and in the non-pregnant groups. Jaundice, digestive tract symptoms, increase of bilirubin and thrombinogen activity were the main manifestations. The incidence of hepatic encephalopathy （HE） and hepato-renal syndrome （HRS） was significantly different between the two groups. The incidence of preterm labor, dead fetus and neonatal asphyxia was high. CONCLUSION： Fulminant hepatitis is likely to occur in late pregnancy wibh more severe complications, which significantly influences maternity, perinatal fetus, and newborn.

Long-term natural history of Crohn’s disease

Crohn’s disease is a chronic inflammatory granulomatous process that usually involves different sites in the intestinal tract. Genetic and environmental factors are thought to play a role in its etiology and pathogenesis. The disorder has a heterogeneous clinical expression and data from tertiary care settings have documented its female predominance, occasional familial nature, and high rate of stricture formation and penetrating disease. It may appear from early childhood to late adulthood, although over 80% are currently diagnosed before age 40 years, usually with terminal ileal and colonic involvement. Several studies have now shown differences in phenotypic clinical expression depending on the initial age at diagnosis, with pediatric-onset disease being more severe and more extensive with more involvement of the upper gastrointestinal tract compared to adult-onset disease. In addition, long- term studies from these tertiary care settings have documented that the disorder may evolve with time into a more complex disease with stricture formation and penetrating disease complications (i.e. fistula and abscess). Although prolonged remission with no evidence of inflammatory disease may occur, discrete periods of symptomatic and active granulomatous inflammatory disease may re-appear over many decades. Long-term studies on the natural history have also suggested that discrete events (or agents) may precipitate this granulomatous inflammatory process.